ArticleBritish journal of pharmacology2003
Protein kinase C-alpha attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 7 citations in OpenAlex.
- Gastric Proton Pumpopathy Associated with Protein Sorting Machinery: A Narrative Review.Clinical and experimental gastroenterology · 2026Review
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
(1) The phorbolester 12-O-tetradecanoyl phorbol-13-acetate (TPA), an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion. We observed that this effect strongly correlated with the inhibition of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity in rabbit parietal cells. (2) The aim of this study was to specify the function of PKC-alpha in cholinergically stimulated H(+) secretion. PKC-alpha represents the only calcium-dependent PKC isoenzyme that has been detected in rabbit parietal cells. (3) Gö 6976, an inhibitor of calcium-dependent PKC, concentration-dependently antagonized the inhibitory effect of TPA, and, therefore, revealed the action of PKC-alpha on carbachol-induced acid secretion in rabbit parietal cells. (4) TPA exerted no additive inhibition of carbachol-stimulated acid secretion if acid secretion was partially inhibited by the potent CaMKII inhibitor 1-[N,O-bis(5-isoquinolinsulfonyl)-N-methyl-L-tyrosyl]-4-phenyl-piperazine (KN-62). (5) Since both kinase modulators, TPA and KN-62, affected no divergent signal transduction pathways in the parietal cell, an in vitro model has been used to study if PKC directly targets CaMKII. CaMKII purified from parietal cell-containing gastric mucosa of pig, was transphosphorylated by purified cPKC containing PKC-alpha up to 1.8 mol P(i) per mol CaMKII in vitro. The autonomy site of CaMKII was not transphosphorylated by PKC. (6) The phosphotransferase activity of the purified CaMKII was in vitro inhibited after transphosphorylation by PKC if calmodulin was absent during transphosphorylation. Attenuation of CaMKII activity by PKC showed strong similarity to the downregulation of CaMKII by basal autophosphorylation. (7) Our results suggest that PKC-alpha and CaMKII are closely functionally linked in a cholinergically induced signalling pathway in rabbit parietal cells. We assume that in cholinergically stimulated parietal cells PKC-alpha transinhibits CaMKII activity, resulting in an attenuation of acid secretion.
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